Accelerated differentiation of melanocyte stem cells contributes to the formation of hyperpigmented maculae.

Accelerated differentiation of melanocyte stem cells contributes to the formation of hyperpigmented maculae.
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黑素细胞干细胞的加速分化有助于色素沉着过度的黄斑的形成。

DOI：
10.1111/exd.12496
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发表时间：
2014
期刊：
Exp Dermatol.
影响因子：
--
通讯作者：
Akamatsu H.
Akamatsu H.
中科院分区：
--
文献类型：
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作者：
Yamada T;Hasegawa S;Inoue Y;Date Y;Arima M;Yagami A;Iwata Y;Takahashi M;Yamamoto N;Mizutani H;Nakata S;Matsunaga K;Akamatsu H.

文献摘要

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据报道，黑色素细胞干细胞（McSCs）的异常调节导致头发变白；然而，对于McSCs在皮肤色素沉着，如太阳色素沉着（SLs）中的作用知之甚少。为了研究McSCs在SL中的作用，我们在UVB诱导的小鼠和人类SL病变中分析了诱发McSCs分化的典型Wnt信号通路。在重复UVB照射后长期形成的HR - 1× HR/De F1小鼠背皮肤上诱导高色素斑后，表皮Wnt1的表达和核β -连环蛋白阳性McSCs的数量较未照射对照小鼠增加。此外，β -连环蛋白的下游靶点多巴胺自变酶（Dct）的表达在UVB照射小鼠的McSCs中显著上调。Wnt1的表达和核β - catenin阳性McSCs的数量在人类SL病变中也高于正常皮肤。重组Wnt1蛋白在早期传代正常人黑素细胞（nhem）、anin体外mcsc模型中诱导黑素细胞相关基因，包括Dct。这些结果表明，典型的Wnt信号通路在SL病变中被激活，并强烈提示McSCs的加速分化参与了SL的发病机制。
It has been reported that the abnormal regulation of melanocyte stem cells (McSCs) causes hair greying; however, little is known about the role of McSCs in skin hyperpigmentation such as solar lentigines (SLs). To investigate the involvement of McSCs in SLs, the canonical Wnt signalling pathway that triggers the differentiation of McSCs was analysed in UVB‐induced delayed hyperpigmented maculae in mice and human SL lesions. After inducing hyperpigmented maculae on dorsal skin of F1 mice of HR‐1× HR/De, which was formed long after repeated UVB irradiation, the epidermal Wnt1 expression and the number of nuclear β‐catenin‐positive McSCs were increased as compared to non‐irradiated control mice. Furthermore, the expression of dopachrome tautomerase (Dct), a downstream target of β‐catenin, was significantly upregulated in McSCs of UVB‐irradiated mice. The Wnt1 expression and the number of nuclear β‐catenin‐positive McSCs were also higher in human SL lesions than in normal skin. Recombinant Wnt1 protein induced melanocyte‐related genes including Dct in early‐passage normal human melanocytes (NHEMs), anin vitroMcSC model. These results demonstrate that the canonical Wnt signalling pathway is activated in SL lesions and strongly suggest that the accelerated differentiation of McSCs is involved in SL pathogenesis.